Monoclonal immunoglobulins (M-proteins) produced by clonal plasma cells are the main cause of multiple myeloma (MM), and hypocomplementemia is observed in some patients with MM. Previous studies have suggested that the glycosylation of immunoglobulins is associated with complement-mediated effector activities. However, the site-specific N-glycosylation of monoclonal immunoglobulins in MM and their effects on complement system activation remain unclear.